Development of an in vivo gene mutation assay using the endogenousPig-Agene: I. Flow cytometric detection of CD59-negative peripheral red blood cells and CD48-negative spleen T-cells from the rat

2008 ◽  
Vol 49 (8) ◽  
pp. 614-621 ◽  
Author(s):  
Daishiro Miura ◽  
Vasily N. Dobrovolsky ◽  
Yoshinori Kasahara ◽  
Yasuhiro Katsuura ◽  
Robert H. Heflich
2008 ◽  
Vol 49 (8) ◽  
pp. 622-630 ◽  
Author(s):  
Daishiro Miura ◽  
Vasily N. Dobrovolsky ◽  
Roberta A. Mittelstaedt ◽  
Yoshinori Kasahara ◽  
Yasuhiro Katsuura ◽  
...  

2012 ◽  
Vol 37 (5) ◽  
pp. 943-955 ◽  
Author(s):  
Takafumi Kimoto ◽  
Satsuki Chikura ◽  
Kumiko Suzuki-Okada ◽  
Xiao-mei Kobayashi ◽  
Yasuhiro Itano ◽  
...  

2016 ◽  
Vol 3 (4) ◽  
pp. 167-175 ◽  
Author(s):  
Jiang Pu ◽  
Yuanyuan Deng ◽  
Xiaoyan Tan ◽  
Gaofeng Chen ◽  
Cong Zhu ◽  
...  

2019 ◽  
Vol 123 ◽  
pp. 424-430 ◽  
Author(s):  
Meirong Qin ◽  
Runhua Chen ◽  
Zeyu Huang ◽  
Jinping Wang ◽  
Suowen Xu ◽  
...  

2011 ◽  
Vol 33 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Katsuyoshi Horibata ◽  
Akiko Ukai ◽  
Naoki Koyama ◽  
Atsuya Takagi ◽  
Jun Kanno ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xuqing Zhang ◽  
Mengyao Luo ◽  
Shamael R. Dastagir ◽  
Mellissa Nixon ◽  
Annie Khamhoung ◽  
...  

AbstractCheckpoint inhibitors and T-cell therapies have highlighted the critical role of T cells in anti-cancer immunity. However, limitations associated with these treatments drive the need for alternative approaches. Here, we engineer red blood cells into artificial antigen-presenting cells (aAPCs) presenting a peptide bound to the major histocompatibility complex I, the costimulatory ligand 4-1BBL, and interleukin (IL)-12. This leads to robust, antigen-specific T-cell expansion, memory formation, additional immune activation, tumor control, and antigen spreading in tumor models in vivo. The presence of 4-1BBL and IL-12 induces minimal toxicities due to restriction to the vasculature and spleen. The allogeneic aAPC, RTX-321, comprised of human leukocyte antigen-A*02:01 presenting the human papilloma virus (HPV) peptide HPV16 E711-19, 4-1BBL, and IL-12 on the surface, activates HPV-specific T cells and promotes effector function in vitro. Thus, RTX-321 is a potential ‘off-the-shelf’ in vivo cellular immunotherapy for treating HPV + cancers, including cervical and head/neck cancers.


2010 ◽  
Vol 51 (8-9) ◽  
pp. 825-835 ◽  
Author(s):  
Vasily N. Dobrovolsky ◽  
Daishiro Miura ◽  
Robert H. Heflich ◽  
Stephen D. Dertinger

2008 ◽  
Vol 27 (3_suppl) ◽  
pp. 59-72 ◽  
Author(s):  
Bruce K. Bernard ◽  
Eri Watanabe ◽  
Terutaka Kodama ◽  
Shoji Tsubuku ◽  
Akira Otabe ◽  
...  

A series of studies was performed to evaluate the safety of dihydrocapsiate (4-hydroxy-3-methoxybenzyl 8-methylnonanoate; CAS no. 205687-03-2). This study evaluated the potential genotoxicity of this compound using a variety of in vitro and in vivo test systems, including bacterial reverse mutation test, chromosomal aberration test, micronucleus test, gene mutation assay with transgenic rats, and single-cell gel (SCG) assay (Comet assay). In vitro tests (bacterial reverse mutation test and chromosomal aberration test) produced positive results in the absence of metabolic activation, but negative results in the presence of metabolic activation. The in vivo gene mutation assay (with transgenic rats) produced negative results, as did the in vivo mouse micronucleus assay, which failed to induce micronucleated polychromatic erythrocytes. Although the rat SCG assay produced statistically significant increases in the Olive tail moment and % tail DNA of the liver and intestine in the 2000 mg/kg group (compared with the negative-control group), a number of factors caused the authors to question the validity of these findings. Taken together, these results suggest that dihydrocapsiate has a low or extremely low likelihood of inducing genotoxicity.


1993 ◽  
Vol 12 (2) ◽  
pp. 155-159 ◽  
Author(s):  
B. Bhaskar Gollapudi ◽  
V. A. Linscombe ◽  
M. L. Mcclintock ◽  
A. K. Sinha ◽  
C. R. Stack

DGBE was evaluated in a forward gene mutation assay at the HGPRT locus of CHO cells in culture and in an in vivo mouse bone marrow micronucleus test for cytogenetic damage. DGBE did not elicit a positive response in the CHO/HGPRT assay when tested up to a maximum concentration of 5000 μg/ml with and without an external metabolic activation system (S-9). In the micronucleus test employing three post-treatment bone marrow sampling times (24, 48, and 72 hr), DGBE was ineffective in increasing the incidence of micronucleated polychromatic erythrocytes (MN-PCE) when tested in both sexes up to a maximum tolerated dose of 3300 mg/kg body weight. Thus, these data and those of others indicate a general lack of genotoxic potential for DGBE in short-term tests.


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